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Anesthesia Considerations for Patients with History of Neck Fracture

Anesthesia Considerations for Patients with Past Neck Fracture

Administering anesthesia to patients with a history of neck fracture presents unique challenges and requires thorough preoperative planning. The cervical spine plays a crucial role in airway management and positioning during anesthesia, and any previous injury to this area may complicate standard protocols. While a healed neck fracture may not present active symptoms, the long-term structural or neurological changes can significantly affect anesthetic risk and technique.

Safe airway management is a core concern during anesthesia for patients with a history of neck fracture. Neck mobility may be limited due to pain, surgical fusion, hardware placement, or residual instability. Limited extension or flexion of the cervical spine can make direct laryngoscopy difficult, increasing the risk of failed intubation or airway trauma. In such cases, alternative airway strategies must be considered. These include the use of video laryngoscopy, fiberoptic bronchoscopy, or even awake intubation if necessary. The objective is to minimize neck movement while securing the airway, reducing the risk of spinal cord injury or exacerbation of an existing condition.

A detailed preoperative assessment is essential. This includes a thorough review of the patient’s medical history, imaging studies such as cervical spine X-rays or MRI, and any prior neurosurgical interventions like fusion or hardware placement. The anesthesiologist should evaluate current neck mobility and neurological status. A history of weakness, numbness, or gait disturbances may indicate underlying instability or chronic spinal cord involvement, which must be factored into the anesthesia plan ^1–5.

Proper positioning during anesthesia and surgery is critical for patients with a history of neck fracture, especially when manipulating the neck. Patients with a past cervical fracture may require additional support to keep the spine aligned during procedures: Foam pads, cervical collars, or custom headrests may be used to prevent unintended movement. Even minor mispositioning can lead to nerve injury or compromise blood flow to the brain and spinal cord in at-risk patients. Extra care may be required during transfers and changes in positioning on the operating table, with close collaboration between surgical and anesthesia teams being essential ^4,5.

The choice between general, regional, or monitored anesthesia care in the context of a history of neck fracture should also be carried out carefully. In many cases, general anesthesia is still appropriate, but modifications may be necessary. Induction agents should be selected to allow for smooth, controlled airway management. If regional anesthesia is considered, such as a nerve block or spinal anesthesia, the patient’s spinal anatomy and neurological status must be carefully evaluated to avoid complications. In some cases, regional techniques may be safer and help avoid airway manipulation altogether, particularly for procedures not involving the head or neck ^6,7.

Patients with a history of neck fracture may be at increased risk for delayed neurological complications. Postoperative monitoring should include neurological status and respiratory function assessments, particularly if the patient’s history includes spinal cord injury. If the procedure involves prolonged neck manipulation or positioning, observation in a recovery unit or intensive care setting may be warranted to ensure no new deficits develop ^7,8.

In summary, anesthesia for patients with a history of neck fracture requires individualized planning, careful airway and positioning strategies, and a thorough understanding of the patient’s cervical spine condition. With appropriate precautions, these patients can safely undergo anesthesia and surgery with minimized risk.

References

1. Ramkumar, V. Preparation of the patient and the airway for awake intubation. Indian J Anaesth 55, 442–447 (2011). DOI: 10.4103/0019-5049.89863

2. Fiberoptic bronchoscopy: Technique, risks, what to expect. https://www.medicalnewstoday.com/articles/fiberoptic-bronchoscopy (2024).

3. Chemsian, R., Bhananker, S. & Ramaiah, R. Videolaryngoscopy. Int J Crit Illn Inj Sci 4, 35–41 (2014). DOI: 10.4103/2229-5151.128011

4. Wiles, M. D. et al. Airway management in patients with suspected or confirmed cervical spine injury. Anaesthesia 79, 856–868 (2024). DOI: 10.1111/anae.16290

5. Austin, N., Krishnamoorthy, V. & Dagal, A. Airway management in cervical spine injury. Int J Crit Illn Inj Sci 4, 50–56 (2014). DOI: 10.4103/2229-5151.128013

6. Folino, T. B. & Mahboobi, S. K. Regional Anesthetic Blocks. in StatPearls (StatPearls Publishing, Treasure Island (FL), 2025).

7. Bao, F., Zhang, H. & Zhu, S. Anesthetic considerations for patients with acute cervical spinal cord injury. Neural Regen Res 12, 499–504 (2017). DOI: 10.4103/1673-5374.202916

8. Dooney, N. & Dagal, A. Anesthetic considerations in acute spinal cord trauma. Int J Crit Illn Inj Sci 1, 36–43 (2011). DOI: 10.4103/2229-5151.79280

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Lidocaine and Tinnitus

Lidocaine is a local anesthetic commonly used across a variety of clinical settings. It can be given intravenously to facilitate tracheal intubation, applied to the gums in dentistry to numb an area prior to a procedure, and administered during surgery to reduce pain and improve outcomes after the operation.¹ Like other local anesthetics, lidocaine binds to sodium channels in nerve cells, preventing nerve depolarization and the transmission of a nerve impulse. Less commonly, lidocaine can be used to manage tinnitus.

Patients with tinnitus hear ringing or other noises without external sources. Often caused by hearing loss or an ear injury, tinnitus can be treated with sound therapies, cognitive behavior therapies, and medications that aid in sleep.² However, there is no FDA-approved drug or treatment specifically for the condition. The need, however, is considerable: according to the American Tinnitus Foundation, 25 million Americans experience some form of the condition, with 2 million, or 8%, finding it debilitating.³

For decades, lidocaine has been observed to temporarily alleviate or dissipate the symptoms of tinnitus. In a 1978 study, the intravenous injection of lidocaine in 78 patients with tinnitus led to the complete disappearance of symptoms in 27 (35%), partial improvement in 22 (28%), and no observed change in 21 (26%).⁴ More recent studies have also demonstrated lidocaine’s positive impact. A 2018 study evaluated an injection of lidocaine with the steroid dexamethasone administered directly into the middle ear through the ear drum (known as an intratympanic injection). Compared to patients who received only dexamethasone, those who received the lidocaine-containing injection experienced improvements in their tinnitus symptoms, as measured by the loudness matching test, in which the volume of an external noise is adjusted to match that of the tinnitus, and the tinnitus handicap index, in which a patient quantifies the difficulties they are experiencing due to tinnitus.⁵

The mechanism by which lidocaine reduces tinnitus symptoms is not entirely clear, but it is thought to relate to the anesthetic’s ability to lower spontaneous hyperactivity in the central nervous system, which can itself be implicated in tinnitus.⁶ Furthermore, lidocaine can improve blood flow to the inner ear and reduce the cochlear microphonic, the electric potential generated by cochlear hair cells in response to sound.⁷

Despite its successes, using lidocaine to treat tinnitus remains imperfect. In fact, it may even have a worsening effect: in one randomized controlled trial, over 30% of patients with tinnitus had worsened symptoms.⁷ Lidocaine can also lead to other side effects, including prolonged numbness, tingling, and slurred speech.

Although lidocaine is not currently recommended for the treatment of tinnitus, recent new approaches in leveraging the anesthetic may help change this. In one study, participants with chronic tinnitus wore a lidocaine patch and had improved symptoms after several months of treatment.⁸ Though the sample size was small, this approach may help represent a new avenue of care for the millions struggling with tinnitus.

References

1. Beecham, G. B., Nessel, T. A. & Goyal, A. Lidocaine. in StatPearls (StatPearls Publishing, Treasure Island (FL), 2025).

2. What Is Tinnitus? — Causes and Treatment | NIDCD. https://www.nidcd.nih.gov/health/tinnitus (2023).

3. What is Tinnitus? | American Tinnitus Association. https://www.ata.org/about-tinnitus/why-are-my-ears-ringing/ (2023).

4. Melding, P. S., Goodey, R. J. & Thorne, P. R. The use of intravenous lignocaine in the diagnosis and treatment of tinnitus. J. Laryngol. Otol. 92, 115–121 (1978), DOI: 10.1017/s002221510008511x

5. Elzayat, S. et al. Evaluation of Adding Lidocaine to Dexamethasone in the Intra-tympanic Injection for Management of Tinnitus: A Prospective, Randomized, Controlled Double-blinded Trial. Int. Tinnitus J. 22, 54–59 (2018), DOI: 10.5935/0946-5448.20180009

6. Kim, S. H. et al. Review of Pharmacotherapy for Tinnitus. Healthcare 9, 779 (2021), DOI: 10.3390/healthcare9060779

7. Duckert, L. G. & Rees, T. S. Treatment of tinnitus with intravenous lidocaine: A double-blind randomized trial. Otolaryngol. Neck Surg. 91, 550–555 (1983), DOI: 10.1177/019459988309100514

8. O’Brien, D. C., Robinson, A. D., Wang, N. & Diaz, R. Transdermal lidocaine as treatment for chronic subjective tinnitus: A Pilot Study. Am. J. Otolaryngol. 40, 413–417 (2019), DOI: 10.1016/j.amjoto.2019.03.009

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Anesthesiology Residency Rotations: A Comprehensive Overview

Anesthesiology residency programs are meticulously structured to provide residents with a broad and in-depth clinical experience. The training typically spans four years: it begins with a Clinical Base Year (PGY-1) and is followed by three years of Clinical Anesthesia (CA-1 to CA-3). Each phase is designed to build upon the previous, ensuring a progressive acquisition of knowledge and skills necessary for competent anesthetic practice. During anesthesiology residency, anesthesiologists-in-training gain experience in diverse clinical settings through rotations and extensive hands-on practice that aim to prepare them for independent practice.

Anesthesiology residency programs are primarily dedicated to cultivating compassionate, knowledgeable, and highly skilled anesthesiologists who can safely and effectively care for patients across a wide range of clinical settings. The mission is to provide comprehensive, progressive training that emphasizes excellence in perioperative medicine, pain management, and critical care ^1,2.

The PGY-1 year serves as the foundation for anesthesiology training, emphasizing the development of general medical knowledge and patient care skills. PGY-1 rotations intersect with various specialties, including internal medicine, surgery, emergency medicine, and critical care, to provide a comprehensive understanding of patient management across various medical disciplines at the start of residency ^3,4.

The CA-1 year marks residents’ immersion into the field of anesthesiology. During this period, residents focus on mastering basic anesthetic techniques and perioperative patient management. This year is pivotal in developing the residents’ proficiency in administering anesthesia and managing patients in the perioperative setting ^5,6.

In the CA-2 year, residents delve into anesthesiology subspecialties, gaining exposure to complex surgical cases and advanced anesthetic techniques. Rotations during anesthesiology residency typically include pediatric anesthesia, obstetric anesthesia, cardiothoracic anesthesia, neuroanesthesia, regional anesthesia, and critical care. This diverse clinical exposure equips residents with the skills necessary to manage a wide array of anesthetic challenges ^7,8.

The final year of residency, CA-3, focuses on refining clinical skills, fostering leadership abilities, and preparing residents for independent practice. Residents often have the opportunity to tailor their rotations based on career interests, engaging in advanced subspecialty rotations, elective experiences, or in-depth research projects. This flexibility allows residents to align their training with future career goals and interests ^9,10.

Anesthesiology residency rotations are thoughtfully designed to provide a comprehensive and progressive training experience. From establishing foundational medical knowledge in the PGY-1 year to refining advanced clinical skills and leadership in the CA-3 year, each phase plays a crucial role in developing competent and confident anesthesiologists. The structured yet flexible nature of these programs ensures that residents are well prepared to meet the diverse challenges of anesthetic practice and to contribute meaningfully to patient care and the broader medical community.

References

1. Miller, J. Mission & Vision – Anesthesiology and Perioperative Medicine. https://www.uab.edu/medicine/anesthesiology/about/mission-vision.

2. Program Mission & Aims » Department of Anesthesiology » College of Medicine » University of Florida. https://anest.ufl.edu/education/residency/program-aims/.

3. Staszak, J. et al. Changing of an anesthesiology clinical base year to create an integrated 48-month curriculum: experience of one program. J Clin Anesth 17, 225–228 (2005). DOI: 10.1016/j.jclinane.2004.08.005

4. Clinical Base Year (PGY-1). Anesthesiology https://www.anesthesiology.cuimc.columbia.edu/education/residency/clinical-anesthesia-rotations/clinical-base-year-pgy-1 (2017).

5. Curriculum | Anesthesia Residency | IU School of Medicine. https://medicine.iu.edu/anesthesia/education/residency/curriculum.

6. Residency Curriculum Overview. https://medicine.yale.edu/anesthesiology/education/resident-life/curriculum/.

7. Program Structure & Rotations – UW Anesthesiology & Pain Medicine. https://anesthesiology.uw.edu/education/residency-program/program-structure-rotations/.

8. Rotations. Dept. of Anesthesiology | GW School of Medicine and Health Sciences https://anesthesiology.smhs.gwu.edu/rotations.

9. Keck School of Medicine of USC Anesthesiology Residency Program. Department of Anesthesiology https://keck.usc.edu/anesthesiology/training-education/keck-school-of-medicine-residency-program/.

10. Curriculum Anesthesiology Residency | Icahn School of Medicine. Icahn School of Medicine at Mount Sinai https://icahn.mssm.edu/education/residencies-fellowships/list/msh-anesthesiology-residency/curriculum.

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Sodium Bicarbonate Adjuvant in Anesthesia

Sodium Bicarbonate Adjuvant in Anesthesia

Sodium bicarbonate, also known as baking soda, is most commonly used in cooking and cleaning, but it has a wide range of medical applications. It’s a basic compound and can therefore neutralize acid indigestion; in this context, it’s known as an antacid. It can also be used to treat acidosis, an excessive buildup of acid in the body’s fluids and tissues. The same principle makes sodium bicarbonate an effective adjuvant in anesthesia.

An adjuvant is a medication given together with a peripheral nerve block, which blocks pain signaling in nerves near the site of surgery and has fewer side effects compared with general anesthesia. An adjuvant can help shorten the time required for onset of analgesia (the inability to feel pain), while also prolonging its duration and depth. Sodium bicarbonate increases the pH of the anesthetic drug, which allows it to more readily exist in its un-ionized, or uncharged, form.¹ In this form, the anesthetic can more easily cross the lipid membrane of peripheral nerves, allowing for a greater analgesic effect and a faster onset.

Sodium bicarbonate has been shown to serve as an effective adjuvant to regional anesthesia in a variety of clinical settings. In one study, investigators added sodium bicarbonate to the anesthetic drugs dexamethasone and ropivacaine for a block of the supraclavicular brachial plexus nerves (which control movement in the upper limb) for upper limb orthopedic surgery.² Patients who received this treatment regimen had quicker onset and longer duration of nerve block compared with the control group. Another trial found that adding sodium bicarbonate to the local anesthetic lignocaine injected into the palate for extraction of the maxillary bilateral premolar teeth reduced pain and shortened the onset of anesthesia, while also increasing its duration.³ The American Society of Anesthesiologists lists a sodium bicarbonate adjuvant as part of its recommendations for the use of adjuvant medications during cesarean delivery (C-section).⁴

However, other studies indicate that sodium bicarbonate may add little to no benefit when used as an adjuvant to anesthesia. One group of investigators found that while sodium bicarbonate leads to a greater reduction of pain in patients undergoing wisdom tooth removal, it made no significant difference in the duration of anesthesia.⁵ Another study in patients undergoing lower extremity surgery observed that sodium bicarbonate did not impact the onset or duration of anesthesia from bupivacaine.⁶

The apparent inconsistencies in when sodium bicarbonate has a significant effect on anesthesia might be a function of which anesthetic is used and where it is administered. One analysis found that it worked best with lidocaine and bupivacaine for epidural block, with lidocaine for brachial plexus block, and with mepivacaine for sciatic and femoral nerve blocks.⁶

Further research into the use of sodium bicarbonate as an adjuvant can not only help guide care providers in providing it to the patients who stand to benefit the most, but it can also help them move away from opioids and the tremendous risk of addiction and overdose they carry. Opioids have traditionally been used as an adjuvant for nerve block,⁷ and they are sometimes used to manage post-operative pain, which sodium carbonate can help alleviate. Thus, sodium bicarbonate may play an important role in reducing the use of opioids in the surgical setting.

References

1. Edinoff, A. N. et al. Adjuvant Drugs for Peripheral Nerve Blocks: The Role of NMDA Antagonists, Neostigmine, Epinephrine, and Sodium Bicarbonate. Anesthesiol. Pain Med. 11, e117146 (2021), DOI: 10.5812/aapm.117146

2. Kour, L., Sharma, G. & Tantray, S. H. Evaluation of Addition of Sodium Bicarbonate to Dexamethasone and Ropivacaine in Supraclavicular Brachial Plexus Block for Upper Limb Orthopedic Procedures. Anesth. Essays Res. 15, 26 (2021), DOI: 10.4103/aer.aer_45_21

3. Gupta, S., Kumar, A., Sharma, A. K., Purohit, J. & Narula, J. S. ‘Sodium bicarbonate’: an adjunct to painless palatal anesthesia. Oral Maxillofac. Surg. 22, 451–455 (2018), DOI: 10.1007/s10006-018-0730-x

4. Statement on the Use of Adjuvant Medications and Management of Intraoperative Pain During Cesarean Delivery. https://www.asahq.org/standards-and-practice-parameters/statement-on-the-use-of-adjuvant-medications-and-management-of-intraoperative-pain-during-cesarean-delivery

5. Shyamala, M. et al. A Comparative Study Between Bupivacaine with Adrenaline and Carbonated Bupivacaine with Adrenaline for Surgical Removal of Impacted Mandibular Third Molar. J. Maxillofac. Oral Surg. 15, 99–105 (2016), DOI: 10.1007/s12663-015-0791-4

6. Candido, K. D. et al. Addition of bicarbonate to plain bupivacaine does not significantly alter the onset or duration of plexus anesthesia. Reg. Anesth. 20, 133–138 (1995).

7. Krishna Prasad, G. V., Khanna, S. & Jaishree, S. V. Review of adjuvants to local anesthetics in peripheral nerve blocks: Current and future trends. Saudi J. Anaesth. 14, 77–84 (2020), DOI: 10.4103/sja.SJA_423_19

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IV Access in Patients with Edema

IV Access in Patients with Edema

Edema, the medical term for swelling, presents unique challenges for healthcare providers when establishing intravenous (IV) access. An understanding of the different types of edema, its underlying etiologies, and the various techniques used to overcome the difficulties it poses for IV cannulation is essential for healthcare providers to provide high-quality care.

Edema occurs when small blood vessels leak fluid into nearby tissues, causing swelling. It can be classified into two main types: pitting and non-pitting edema. Pitting edema leaves an indentation when pressure is applied to the affected area, while non-pitting edema does not. Dependent edema, a subtype of pitting edema, occurs in the lower extremities due to gravity and is common in bedridden patients or those with prolonged standing. In addition to the lower extremities, the hips are another site where dependent edema is commonly seen.

While there are numerous causes of edema, two primary mechanisms include low oncotic pressure and volume overload. Hypoalbuminemia, a condition characterized by low levels of albumin in the blood, reduces plasma oncotic pressure, leading to fluid retention in subcutaneous tissues and edema formation. Volume overload, on the other hand, can result from conditions such as heart failure or renal failure, where the body retains excess fluid due to impaired regulatory mechanisms. As a result of this excessive fluid, patients develop edema due to high hydrostatic pressures in the blood vessels.

Edema presents significant technical challenges for IV access. The swollen tissue obscures normal anatomical landmarks, making vein identification difficult. The increased tissue pressure can compress veins, reducing their diameter and making them harder to puncture. Additionally, the excess fluid in the tissues can cause the needle to deviate from its intended path, increasing the risk of failed cannulation attempts.

To overcome these challenges, healthcare providers employ various methods for obtaining IV access in patients with edema. The traditional free-hand method, while still used, is often less effective in these cases. Ultrasound-guided techniques have emerged as a valuable tool for vascular access in difficult cases. By providing real-time visualization of the vein and surrounding structures, ultrasound guidance improves success rates and reduces complications.

When peripheral IV access proves challenging or impossible, more invasive options may be considered. Peripherally inserted central catheters (PICC lines) offer a longer-term solution for patients requiring extended IV therapy. Central venous catheters, inserted into large veins in the neck, chest, or groin, are used when peripheral access is not feasible or when rapid infusion of large volumes is necessary. These options are particularly useful in patients with severe edema or those requiring long-term IV therapy.

The choice of IV access method in patients with edema depends on several factors, including the severity of edema, the expected duration of IV therapy, and the patient’s overall condition. In all cases, careful assessment and skilled technique are essential to minimize complications and ensure successful vascular access.

In conclusion, edema significantly complicates IV access, requiring healthcare providers to adapt their techniques and consider alternative approaches. Understanding the pathophysiology of edema and mastering advanced cannulation methods are crucial for providing optimal care to these challenging patients.

References

Trayes KP, Studdiford JS, Pickle S, Tully AS. Edema: diagnosis and management. Am Fam Physician. 2013;88(2):102-110. https://www.aafp.org/pubs/afp/issues/2013/0715/p102.html
Cho S, Atwood JE. Peripheral edema. Am J Med. 2002;113(7):580-586. doi: 10.1016/s0002-9343(02)01322-0
Levitt DG, Levitt MD. Human serum albumin homeostasis: a new look at the roles of synthesis, catabolism, renal and gastrointestinal excretion, and the clinical value of serum albumin measurements. Int J Gen Med. 2016;9:229-255. doi: 10.2147/IJGM.S102819
Sterns RH. Pathophysiology and etiology of edema in adults. UpToDate. Accessed March 22, 2025. https://www.uptodate.com/contents/pathophysiology-and-etiology-of-edema-in-adults
Lamperti M, Bodenham AR, Pittiruti M, et al. International evidence-based recommendations on ultrasound-guided vascular access. Intensive Care Med. 2012;38(7):1105-1117. doi: 10.1007/s00134-012-2597-x

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Airway Management: Anatomy of the Airway

Airway Management: Anatomy of the Airway

Airway management is a crucial aspect of medical practice, particularly in emergency situations, anesthesia, and critical care, making it essential for healthcare providers to understand the anatomy of the airway. The airway consists of both upper and lower respiratory structures, and each part plays a significant role in the passage of air from the environment to the lungs.

Upper airway anatomy consists of several key structures relevant for airway management due to their roles in directing air to the lungs while also filtering, warming, and humidifying it. The first part of the upper airway is the nasal cavity, where air is first drawn in. The nasal passages are lined with mucous membranes that trap debris and pathogens before they can enter the lungs. From the nasal cavity, air passes through the nasopharynx, the upper portion of the throat located behind the nose. The nasopharynx is followed by the oropharynx, which serves as a passageway for both air and food. It is located behind the mouth and contains structures such as the uvula, tonsils, and the base of the tongue. Next, at the laryngopharynx, the pathways for air and food diverge. The larynx, or voice box, sits at the junction of the laryngopharynx and the trachea and contains the vocal cords. It is involved in breathing, swallowing, and vocalizing. The epiglottis, a flap of tissue located above the larynx, acts as a protective mechanism by closing off the airway during swallowing to prevent food or liquids from entering the trachea ^1–3.

The lower airway begins at the trachea, a rigid, cartilaginous tube lined with mucous membranes and cilia that help trap and move foreign particles out of the airway. It extends from the larynx down to the level of the carina, where it bifurcates into the left and right mainstem bronchi. The right mainstem bronchus is shorter and more vertically oriented than the left, which makes it more prone to accidentally being intubated in emergency situations. Each mainstem bronchus branches into secondary and tertiary bronchi, further dividing into smaller airways known as bronchioles—the smallest branches of the airways that lead to the alveoli, which are surrounded by a network of capillaries where oxygen is transferred into the bloodstream and carbon dioxide is removed from the body ^1,2,4.

Airway management requires that the patient’s airway remains open and unobstructed. In an emergency, providers may need to secure the airway through interventions such as endotracheal intubation, where a tube is inserted into the trachea to maintain airflow. In addition, in situations of respiratory distress or failure, the management of the airway can include using mechanical ventilation to assist or replace normal breathing. Effective airway management is essential not only for maintaining oxygenation but also for preventing complications like aspiration, which can lead to pneumonia or other respiratory issues. A thorough understanding of the anatomy of the airway is vital for healthcare providers, as it enables them to quickly assess the situation and make informed decisions about the best approach to airway management and the maintenance of adequate respiratory function ^5–7.

References

1. What Are Your Airways? Cleveland Clinic https://my.clevelandclinic.org/health/body/airway.

2. Ball, M., Hossain, M. & Padalia, D. Anatomy, Airway. in StatPearls (StatPearls Publishing, Treasure Island (FL), 2025).

3. Upper Respiratory Airways. Physiopedia https://www.physio-pedia.com/Upper_Respiratory_Airways.

4. Lower respiratory tract: MedlinePlus Medical Encyclopedia Image. https://medlineplus.gov/ency/imagepages/19379.htm.

5. Avva, U., Lata, J. M. & Kiel, J. Airway Management. in StatPearls (StatPearls Publishing, Treasure Island (FL), 2025).

6. Jacobs, L. M. The Importance of Airway Management in Trauma. J Natl Med Assoc 80, 873–879 (1988).

7. Trauma Service : Airway management. https://www.rch.org.au/trauma-service/manual/airway-management/.

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Treatment of Fluid Retention During Surgery

Treatment of Fluid Retention During Surgery

Fluid retention during surgery poses a significant challenge to perioperative management because excessive fluid accumulation can impair organ function and wound healing and increase morbidity. Effective strategies for managing fluid retention during surgery involve a combination of precise fluid administration, pharmacologic intervention, and vigilant monitoring of physiological parameters to maintain hemodynamic stability while avoiding complications such as edema and electrolyte imbalance.

Surgery causes significant physiological stress that triggers the release of hormones such as aldosterone and antidiuretic hormone (ADH). These hormones promote fluid retention by increasing sodium and water reabsorption in the kidneys. At the same time, surgical trauma activates an inflammatory response that increases capillary permeability and allows fluid to leak into the tissues. This fluid shift can cause swelling (edema) and reduce circulating blood volume. To address these challenges, clinicians can use balanced crystalloids instead of saline as intravenous (IV) fluids. Balanced crystalloids prevent complications such as hyperchloremic acidosis that can occur with excessive saline use (1). Advanced hemodynamic monitoring tools, including cardiac output and stroke volume analysis, help guide fluid administration to maintain balance without overloading or depleting the patient’s fluid reserves.

Pharmacologic intervention is critical in the management of fluid retention during and after surgery, especially in patients predisposed to complications such as those with heart failure or chronic kidney disease. Diuretics, such as furosemide, are commonly used to promote urinary excretion of excess fluid. However, they must be used with caution, as excessive diuresis can lead to dehydration and electrolyte disturbances, including low potassium or sodium levels. Electrolyte monitoring and repletion are often required to address these issues (2). In cases of significant fluid retention or dilutional hyponatremia, vasopressin receptor antagonists offer a targeted solution. These drugs block fluid retention without disrupting sodium balance, making them particularly useful in complex surgeries such as liver transplantation or cardiac surgery (3).

Minimizing surgical trauma is another effective way to reduce fluid retention. Minimally invasive techniques, such as laparoscopic or robotic surgery, cause less tissue damage than traditional open surgery. This reduces the inflammatory response and associated capillary leakage, resulting in better fluid management and faster recovery. Perioperative measures such as maintaining normothermia also play a vital role. Hypothermia during surgery can impair renal function and exacerbate fluid retention through vasoconstriction and hormonal imbalance. Techniques such as warming blankets, heated IV fluids, and active warming devices help maintain body temperature and mitigate these effects.

For severe cases of fluid retention, especially in patients with acute kidney injury or refractory fluid overload, continuous renal replacement therapy (CRRT) is an advanced treatment option. CRRT is a form of dialysis that removes excess fluid and toxins while maintaining electrolyte balance. It is particularly useful in critically ill patients who cannot tolerate traditional diuretic therapy. Early implementation of CRRT has been shown to improve outcomes by allowing gradual fluid removal without causing hemodynamic instability (4).

In conclusion, the management of fluid retention during surgery is a multifaceted process that requires precision and adaptability. By combining tailored fluid therapy, pharmacologic interventions, minimally invasive techniques, and innovative monitoring, clinicians can effectively address the challenges posed by fluid retention. These evidence-based strategies improve surgical outcomes, enhance recovery, and reduce the risk of complications, demonstrating the importance of a proactive approach to perioperative care.

References

Myburgh JA, Mythen MG. Resuscitation fluids. N Engl J Med. 2013;369(13):1243-1251. doi:10.1056/NEJMra1208627
Kellum JA, Lameire N; KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care. 2013;17(1):204. Published 2013 Feb 4. doi:10.1186/cc11454
Schrier RW. Water and sodium retention in edematous disorders: role of vasopressin and aldosterone. Am J Med. 2006;119(7 Suppl 1):S47-S53. doi:10.1016/j.amjmed.2006.05.007
Hoste EA, Bagshaw SM, Bellomo R, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41(8):1411-1423. doi:10.1007/s00134-015-3934-7

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Factors Affecting Propofol Injection Pain

Factors Affecting Propofol Injection Pain

Propofol is a commonly used intravenous anesthetic, popular for its rapid onset and effectiveness in inducing sedation and analgesia. However, one of the challenges associated with propofol administration is propofol injection pain. This discomfort, which occurs in 28%–90% of patients according to studies of different patient groups,1 can be distressing and complicates the overall experience of medical procedures. Several different factors, such as pharmacodynamics, the rate of injection, and patient-specific variables, can all play significant roles in the intensity and frequency of propofol injection pain. Understanding the mechanisms underlying this pain is crucial for improving surgical flow and patient outcomes in clinical settings.

A 2008 study found transient receptor potential ankyrin 1 (TRPA1), a nonselective ligand-gated cation channel, is heavily involved in the activation of peripheral nerve endings by general anesthetics, including propofol. TRPA1 is an ion channel on cell plasma membranes that is associated with pain perception; it is known as a biological sensor for chemical irritants, oxidative stress, and colder temperatures. In wild-type mice, propofol was shown to produce pain-related behaviors. In contrast, nocifensive behavior was absent in TRPA1–/− mice, but not in TRPA1+/− littermates. Propofol, when injected into the femoral artery, evoked reflex muscle activity in TRPA1+/− but not in their TRPA1–/− counterparts. These results indicate having one allele of the TRPA1 gene is sufficient for propofol-induced injection pain.2

A later study found another potential causative agent: transient receptor ankyrin vanilloid 1 (TRPV1), the excitatory ion channel of the transient receptor potential family that is activated by noxious stimuli such as capsaicin, protons, and excessive heat. The study, performed on human cell TRPA1 and TRPV1, revealed the two molecules mediate propofol-induced injection pain through increasing calcium ions in the dorsal root ganglion.3 This molecular release induces vascular leakage and is thought to contribute to neurogenic inflammation in the periphery and central sensitization in the spinal dorsal horn.1

The speed of injection and site of administration are also factors influencing propofol injection pain. Slow injection causes more pain than rapid bolus since slow injection increases the concentration and duration of exposure of propofol to the vein wall, while rapid injection quickly clears the drug from the vein and replaces it with blood.4 It is suggested the painful sensation originates from neural elements within the vein wall by way of free afferent nerve endings. Propofol

administration can release kininogen, the precursor to bradykinin, which supports vasodilation and hyper-permeability. Prolonged propofol administration may increase interaction between the drug and bradykinin, causing pain, swelling, and inflammation.5 In a prospective cohort study where patients were separated by age and gender, male subjects receiving propofol through the top of the hand were much less likely to experience propofol injection pain than their female counterparts (45.7% vs 74%). However, all groups demonstrated a significant decrease in propofol injection pain when the site of administration changed from the dorsum of hand to the antecubital fossa, i.e., the inside of the elbow (12.5% for men and 37% for women).6

While propofol remains a widely used and highly effective anesthetic, propofol injection pain is an important side effect to research and address in order to improve patient comfort. The multifaceted nature of propofol injection pain, involving both pharmacological and procedural factors, underscores the complexity and necessity of managing this side effect. Although there has been some research conducted to identify key contributors to this pain, it remains an area that requires deeper investigation. Additionally, much of the research to date is based on older datasets, highlighting the need for more contemporary studies to build on earlier findings.

References

1. Desousa, Kalindi A., “Pain on Propofol Injection: Causes and Remedies.” Indian Journal of Pharmacology, vol. 48, no. 6, 2016, p. 617. https://doi.org/10.4103/0253-7613.194845

2. Matta, José A., et al. “General Anesthetics Activate a Nociceptive Ion Channel to Enhance Pain and Inflammation.” Proceedings of the National Academy of Sciences, vol. 105, no. 25, June 2008, pp. 8784–89. https://doi.org/10.1073/pnas.0711038105

3. Fischer, Michael J. M., et al. “The General Anesthetic Propofol Excites Nociceptors by Activating TRPV1 and TRPA1 Rather than GABAA Receptors.” The Journal of Biological Chemistry, vol. 285, no. 45, Sept. 2010, p. 34781. https://doi.org/10.1074/jbc.M110.143958

4. Scott, R. P., et al. “Propofol: Clinical Strategies for Preventing the Pain of Injection.” Anaesthesia, vol. 43, no. 6, June 1988, pp. 492–94. https://doi.org/10.1111/j.1365-2044.1988.tb06641.x

5. Leff, Phillip J., et al. “Characteristics That Increase the Risk for Pain on Propofol Injection.” BMC Anesthesiology, vol. 24, no. 1, May 2024, p. 190. https://doi.org/10.1186/s12871-024-02573-y.

6. Kang, Hye-Joo, et al. “Clinical Factors Affecting the Pain on Injection of Propofol.” Korean Journal of Anesthesiology, vol. 58, no. 3, Mar. 2010, pp. 239–43. https://doi.org/10.4097/kjae.2010.58.3.239

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Anesthetics with the Least Hemodynamic Effects

Anesthetics with the Least Hemodynamic Effects

Certain anesthetic agents can have significant effects on the cardiovascular system, causing changes in heart rate, blood pressure, and cardiac output. For patients with cardiovascular disease or other conditions that make them sensitive to hemodynamic fluctuations, choosing anesthetics with the least hemodynamic effects is essential for reducing the risk of complications.

Hemodynamic effects refer to changes in the circulatory system, particularly those related to heart function and blood flow. Anesthetic agents can cause a variety of hemodynamic changes, including hypotension, bradycardia, or tachycardia 1–3. These effects can be dangerous for patients with compromised cardiovascular function, such as those with coronary artery disease, heart failure, or severe hypertension. For these patients, anesthetics that have the least hemodynamic effects are preferred to reduce the risk of perioperative cardiovascular events, including heart attack and stroke.

Several anesthetic agents are known for their minimal effects on the cardiovascular system, making them ideal for use in high-risk patients. These agents include certain intravenous and inhaled anesthetics as well as local anesthetics used for regional blocks.

Dexmedetomidine is a sedative and anesthetic agent that has gained popularity due to its ability to provide sedation and pain relief with minimal hemodynamic effects. It acts as an alpha-2 adrenergic agonist, leading to a reduction in sympathetic nervous system activity, which can help prevent significant fluctuations in heart rate and blood pressure. Unlike other sedatives, such as propofol, dexmedetomidine tends to cause only mild hypotension and bradycardia without suppressing respiratory function, making it an excellent choice for patients with cardiovascular risk factors 4.

Etomidate is an intravenous anesthetic agent commonly used for induction in patients with hemodynamic instability. It is known for its ability to induce anesthesia rapidly without causing significant changes in heart rate, blood pressure, or cardiac output. Unlike other induction agents like propofol or thiopental, which can cause hypotension, etomidate maintains cardiovascular stability, making it especially useful in patients with heart failure or shock 5.

Midazolam, a benzodiazepine, is another agent with minimal hemodynamic effects. It is often used for preoperative sedation and as an adjunct in anesthesia protocols. While midazolam can cause mild hypotension in some cases, it generally has a favorable cardiovascular profile compared to other sedatives and is often used in patients with cardiovascular concerns. It is commonly administered alongside other agents for balanced anesthesia 6.

Sevoflurane is a widely used inhaled anesthetic with a relatively low impact on the cardiovascular system compared to other volatile anesthetics. It causes less myocardial depression and minimal vasodilation, leading to more stable blood pressure and heart rate during anesthesia. Sevoflurane is particularly useful for maintaining anesthesia in patients who require careful management of their cardiovascular status 7.

Local anesthetics used for regional anesthesia, such as bupivacaine and ropivacaine, have minimal systemic hemodynamic effects when used in appropriate doses 8,9.

For patients with cardiovascular concerns or those at risk of hemodynamic instability, selecting anesthetics with the least effects on blood pressure, heart rate, and cardiac output is essential for ensuring a safe surgical experience.

References

1. Barker, S. J., Gamel, D. M. & Tremper, K. K. Cardiovascular effects of anesthesia and operation. Critical Care Clinics (1987). doi:10.1016/s0749-0704(18)30545-1

2. Ebert, T. J. Sympathetic and hemodynamic effects of moderate and deep sedation with propofol in humans. Anesthesiology (2005). doi:10.1097/00000542-200507000-00007

3. Hemodynamic management during anesthesia in adults – UpToDate. Available at: https://www.uptodate.com/contents/hemodynamic-management-during-anesthesia-in-adults.

4. Dexmedetomidine – StatPearls – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK513303/.

5. Etomidate – StatPearls – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK535364/.

6. Midazolam – StatPearls – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK537321/.

7. Sevoflurane – StatPearls – NCBI Bookshelf. Available at: https://www.ncbi.nlm.nih.gov/books/NBK534781/.

8. Rutten, A. J. et al. Hemodynamic and central nervous system effects of intravenous bolus doses of lidocaine, bupivacaine, and ropivacaine in sheep. Anesth. Analg. (1989). doi:10.1213/00000539-198909000-00004

9. Hashemian, M. et al. Comparison of Ropivacaine versus Bupivacaine in Spinal-Induced Hypotension in Preeclampsia Patients: A Randomized Control Trial. Anesthesiol. Pain Med. 14, (2024). doi: 10.5812/aapm-14264

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Fall vs. Spring Allergies

Fall vs. Spring Allergies

Allergies are a common seasonal issue that affect millions of people worldwide. While many associate allergies primarily with the spring, fall allergies can be just as troublesome. Both seasons bring specific allergens that can trigger symptoms such as sneezing, runny nose, itchy eyes, and congestion.

Spring allergies are predominantly triggered by pollen. As trees, grasses, and flowers begin to bloom in warming weather, they release large amounts of pollen into the air. Common culprits include trees like oak, birch, maple, and various grasses. Pollen levels typically peak in the morning and on dry, windy days when pollen is easily dispersed through the air.

For those with pollen allergies, springtime can be particularly challenging. Pollen grains are small and lightweight, allowing them to travel long distances and penetrate deep into the respiratory system. When an allergic person inhales pollen, their immune system mistakenly identifies it as a harmful substance, triggering a cascade of symptoms. This condition, commonly known as hay fever or allergic rhinitis, can significantly affect daily life, leading to fatigue and decreased productivity ^1–3.

Fall allergies are primarily caused by ragweed pollen, mold, and dust mites. Ragweed is a resilient plant that grows abundantly in many regions, and it produces a significant amount of pollen from late summer into the fall. Ragweed pollen can travel hundreds of miles in the air, making it difficult to escape, even in urban areas.

Mold is another common allergen in the fall, especially in damp and decaying leaves, soil, and compost piles. As temperatures cool and humidity levels rise, mold spores proliferate, becoming airborne and triggering allergic reactions. Dust mites, although present year-round, tend to become more problematic in the fall when homes are closed up and heating systems are turned on, stirring up dust and allergens trapped inside ^4,5.

Tree and grass pollen are the main spring allergens, while ragweed pollen, mold, and dust mites are the primary fall allergens. Spring allergies often cause more upper respiratory symptoms, such as sneezing, itchy eyes, and a runny nose while fall allergies can lead to more lower respiratory symptoms, as well as trigger indoor allergies as people spend more time inside with closed windows, increasing exposure to dust mites and mold ^6,7.

Regardless of the season, managing allergies effectively requires a combination of strategies. First, limiting exposure to allergens is crucial. During peak pollen seasons, keep windows closed and use air conditioning with a clean filter. For mold, regularly clean and dry areas prone to dampness, such as basements and bathrooms ⁸.

Second, environmental control measures can be taken. For example, individuals can use high-efficiency particulate air (HEPA) filters to reduce airborne allergens in the home. Regularly washing bedding and vacuuming with a HEPA filter vacuum cleaner can also minimize exposure to dust mites ⁹.

Finally, over-the-counter antihistamines, decongestants, and nasal corticosteroids can help alleviate symptoms. For more severe cases, a doctor may prescribe stronger medications or recommend allergy shots (immunotherapy) to build tolerance to specific allergens ¹⁰.

Both fall and spring allergies present unique challenges, but understanding their causes and symptoms can help sufferers manage their condition more effectively. Whether dealing with pollen in the spring or ragweed and mold in the fall, taking proactive steps can reduce the impact of seasonal allergies and improve overall quality of life.

References

1. The Spring Allergy: What Causes Sneezing and Runny Eyes. Available at: https://www.webmd.com/allergies/spring-allergies.

2. Spring allergies: Causes, management, and home remedies. Available at: https://www.medicalnewstoday.com/articles/spring-allergies.

3. Allergic Rhinitis (Hay Fever): Symptoms & Treatment. Available at: https://my.clevelandclinic.org/health/diseases/8622-allergic-rhinitis-hay-fever.

4. Fall Allergies: Symptoms and 8 Causes. Available at: https://health.clevelandclinic.org/remedies-for-fall-allergies.

5. Fall Allergies. Available at: https://www.webmd.com/allergies/fall-allergy-relief.

6. Fall vs. spring allergies: What is the difference? Available at: https://www.medicalnewstoday.com/articles/fall-allergies-vs-spring#symptoms.

7. The Difference Between Spring and Fall Allergies – Coastal Ear, Nose & Throat. Available at: https://coastal-ent.com/posts/allergies/the-difference-between-spring-and-fall-allergies/.

8. What triggers seasonal allergies? | NIH MedlinePlus Magazine. Available at: https://magazine.medlineplus.gov/article/what-triggers-seasonal-allergies.

9. The 8 Best Air Purifiers for Allergies of 2024. Available at: https://www.verywellhealth.com/best-air-purifiers-for-allergies-4170072.

10. Seasonal Allergies (Allergic Rhinitis) > Fact Sheets > Yale Medicine. Available at: https://www.yalemedicine.org/conditions/seasonal-allergies.